A neurobiological model of the brain emotional systems has been proposed to explain the persistent changes in motivation that are associated with vulnerability to relapse in addiction, and this model may generalize to other psychopathology associated with dysregulated motivational systems. In this framework, addiction is conceptualized as a cycle of decreased function of brain reward systems and recruitment of antireward systems that progressively worsen, resulting in the compulsive use of drugs. Counteradaptive processes, such as opponent process, that are part of the normal homeostatic limitation of reward function fail to return within the normal homeostatic range and are hypothesized to repeatedly drive the allostatic state. Excessive drug taking thus results in not only the short-term amelioration of the reward deficit but also suppression of the antireward system. However, in the long term, there is worsening of the underlying neurochemical dysregulations that ultimately form an allostatic state (decreased dopamine and opioid peptide function, increased corticotropin-releasing factor activity). This allostatic state is hypothesized to be reflected in a chronic deviation of reward set point that is fueled not only by dysregulation of reward circuits per se but also by recruitment of brain and hormonal stress responses. Vulnerability to addiction may involve genetic comorbidity and developmental factors at the molecular, cellular, or neurocircuitry levels that sensitize the brain antireward systems.

中文翻译：

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成瘾和大脑的抗奖赏制度。

已经提出了一种大脑情绪系统的神经生物学模型来解释与成瘾复发易感性相关的动机的持续变​​化，并且该模型可以推广到与动机系统失调有关的其他心理病理学。在这种框架下，成瘾被概念化为一个循环，即大脑奖励系统功能下降和募集的抗奖赏系统逐渐恶化，导致强制使用药物。作为奖励功能的正常体内平衡限制的一部分的反适应过程（例如对手过程）无法在正常体内平衡范围内返回，并被假设为反复驱动该稳态。因此，过度吸毒不仅会短期改善奖励不足，还会抑制抗奖赏制度。但是，从长远来看，潜在的神经化学失调会恶化，最终形成同种异体状态（多巴胺和阿片肽功能降低，促肾上腺皮质激素释放因子活性增加）。据推测，这种同种异体状态反映在奖励设定点的长期偏离中，这不仅是由于奖励回路本身失调引起的，而且还因大脑和激素应激反应的募集而加剧。上瘾的脆弱性可能涉及使大脑抗奖赏系统敏感的分子，细胞或神经回路水平的遗传合并症和发育因素。最终形成同种异体状态的潜在神经化学失调加剧（多巴胺和阿片肽功能降低，促肾上腺皮质激素释放因子活性增加）。据推测，这种同种异体状态反映在奖励设定点的长期偏离中，这不仅是由于奖励回路本身失调引起的，而且还因大脑和激素应激反应的募集而加剧。上瘾的脆弱性可能涉及使大脑抗奖赏系统敏感的分子，细胞或神经回路水平的遗传合并症和发育因素。最终形成同种异体状态的潜在神经化学失调加剧（多巴胺和阿片肽功能降低，促肾上腺皮质激素释放因子活性增加）。据推测，这种同种异体状态反映在奖励设定点的长期偏离中，这不仅是由于奖励回路本身失调引起的，而且还因大脑和激素应激反应的募集而加剧。上瘾的脆弱性可能涉及使大脑抗奖赏系统敏感的分子，细胞或神经回路水平的遗传合并症和发育因素。据推测，这种同种异体状态反映在奖励设定点的长期偏离中，这不仅是由于奖励回路本身失调引起的，而且还因大脑和激素应激反应的募集而加剧。上瘾的脆弱性可能涉及使大脑抗奖赏系统敏感的分子，细胞或神经回路水平的遗传合并症和发育因素。据推测，这种同种异体状态反映在奖励设定点的长期偏离中，这不仅是由于奖励回路本身失调引起的，而且还因大脑和激素应激反应的募集而加剧。上瘾的脆弱性可能涉及使大脑抗奖赏系统敏感的分子，细胞或神经回路水平的遗传合并症和发育因素。